Near‐complete adaptation of the PRiMA knockout to the lack of central acetylcholinesterase

0301 basic medicine Pyridines Microdialysis Cholinergic Agents Muscle Proteins Membrane Potentials Body Temperature Choline Mice Receptors Scopolamine Hydrobromide Gait Neurons Ingrown Heterocyclic Statistics Brain Adaptation, Physiological Neostigmine 3. Good health Spinal Cord Acetylcholinesterase [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC] Collagen Drug Protein Binding Physiological Knockout 610 Nerve Tissue Proteins Muscarinic Antagonists Motor Activity In Vitro Techniques Tritium Dose-Response Relationship Bridged Bicyclo Compounds 03 medical and health sciences Muscarinic Animals Nonparametric [SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC] Adaptation Maze Learning Radioisotopes Dose-Response Relationship, Drug Membrane Proteins Pirenzepine Dihydro-beta-Erythroidine Newborn Bridged Bicyclo Compounds, Heterocyclic Bungarotoxins Acetylcholine Nails Animals, Newborn Gene Expression Regulation Rotarod Performance Test Exploratory Behavior Cholinesterase Inhibitors
DOI: 10.1111/j.1471-4159.2012.07856.x Publication Date: 2012-07-02T20:54:02Z
ABSTRACT
Acetylcholinesterase (AChE) rapidly hydrolyzes acetylcholine. At the neuromuscular junction, AChE is mainly anchored in extracellular matrix by collagen Q, whereas brain, tethered proline-rich membrane anchor (PRiMA). The AChE-deficient mice, which has been deleted from all tissues, have severe handicaps. Surprisingly, PRiMA KO mice mostly eliminated brain show very few deficits. We now report that most of changes observed and particular high levels ambient acetylcholine massive decrease muscarinic receptors, are also KO. However, two groups mutants differ their responses to inhibitors. Since PRiMA-KO similar low concentrations but content peripheral nervous system, these results suggest system a major target inhibitors, its absence AChE- deficient main cause slow development vulnerability mice. level adaptation nearly complete.
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